Susceptibility to provoked cerebral infarction is not increased in a rat model of pharmacologically-induced hypertension despite endothelial dysfunction.

— An increase in susceptibility to provoked stroke has been described in a genetically-determined rat model of hypertension. We investigated whether the susceptibility to provoked cerebral ischaemia was also increased in a rat model of pharmacologically-induced hypertension with endothelial dysfunction. Chronic inhibition of nitric oxide synthase induced by Nω-nitro-L-arginine methyl ester (L-NAME) administration (50 or 75 mg. kg−1 day−1) in drinking water for 6 weeks caused a sustained hypertension, comparable in the two groups. Endothelium-dependent relaxation induced by acetylcholine or A22187 was significantly, and dose-dependently, impaired in rats receiving L-NAME, as proven by a decrease in maximal relaxation and increase of EC50, as compared to control. Endothelium-independent relaxation induced by sodium nitroprusside was not different in the three groups. Aortic media area was significantly, and dose-dependently, increased following chronic nitric oxide inhibition. Cerebral infarct volumes were not increased in L-NAME-treated groups independently of the level of endothelial dysfunction induced by chronic L-NAME administration. These data demonstrate that susceptibility to cerebral infarction was not increased in a non-genetically determined hypertension model in spite of the development of endothelial dysfunction and vascular structure alterations.